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Mesenchymal transition and acquired therapy resistance of glioblastoma cells is connected to astrocyte reactivity (Affymetrix HTA 2.0 data set)

ABSTRACT: We show that Glioma initiating cells (GICs) can, through MES transition, enter a reactive-astrocyte-like cell state which is connected to increased therapy resistance

ORGANISM(S): Homo sapiens

PROVIDER: GSE122807 | GEO | 2020/11/30

REPOSITORIES: GEO

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Mesenchymal transition and acquired therapy resistance of glioblastoma cells is connected to astrocyte reactivity (DNA methylation data set)

Project description:We show that Glioma initiating cells (GICs) can, through MES transition, enter a reactive-astrocyte-like cell state which is connected to increased therapy resistance

2020-11-30 | GSE122808 | GEO

Mesenchymal transition and acquired therapy resistance of glioblastoma cells is connected to astrocyte reactivity (Affymetrix HTA 2.0 data set)

Project description:Mesenchymal transition and acquired therapy resistance of glioblastoma cells is connected to astrocyte reactivity (Affymetrix HTA 2.0 data set)

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Mesenchymal transition and acquired therapy resistance of glioblastoma cells is connected to astrocyte reactivity

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-11-30 | GSE122809 | GEO

Mesenchymal transition and acquired therapy resistance of glioblastoma cells is connected to astrocyte reactivity

Project description:Mesenchymal transition and acquired therapy resistance of glioblastoma cells is connected to astrocyte reactivity

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A Molecular Switch for Neuroprotective Astrocyte Reactivity

Project description:Astrocytes differentiate into a spectrum of neurotoxic and neuroprotective reactive subpopulations after CNS injury and in disease. In astrocyte conditional ADCY10 (sAC) knockout mice, reactive astrocytes exhibit a shift towards neurotoxic phenotypes implicating sAC as a critical regulator of neuroprotective astrocyte differentiation.

2023-12-11 | GSE237675 | GEO

A Molecular Switch for Neuroprotective Astrocyte Reactivity

Project description:The intrinsic mechanisms that regulate neurotoxic versus neuroprotective astrocyte phenotypes and their effects on central nervous system (CNS) degeneration and repair remain poorly understood. Here, we show injured white matter astrocytes differentiate into two distinct C3-positive and C3-negative reactive populations, previously simplified as neurotoxic (A1) and neuroprotective (A2)1,2, which can be further subdivided into unique subpopulations defined by proliferation and differential gene expression signatures. We find the balance of neurotoxic versus neuroprotective astrocytes is regulated by discrete pools of compartmented cAMP derived from soluble adenylyl cyclase (sAC) and show proliferating neuroprotective astrocytes inhibit microglial activation and downstream neurotoxic astrocyte differentiation to promote retinal ganglion cell (RGC) survival. Finally, we report a new, therapeutically tractable viral vector to specifically target optic nerve head astrocytes and show elevating nuclear or depleting cytoplasmic cAMP in reactive astrocytes inhibits deleterious immune cell infiltration and promotes RGC survival after optic nerve injury. Thus, soluble adenylyl cyclase and compartmented, nuclear- and cytoplasmic-localized cAMP in reactive astrocytes act as a molecular switch for neuroprotective astrocyte reactivity that can be targeted to inhibit microglial activation and neurotoxic astrocyte differentiation to therapeutic effect. These data expand upon and define new reactive astrocyte subtypes and represents a novel step towards the development of gliotherapeutics for the treatment of glaucoma and other optic neuropathies.

2023-12-11 | GSE245816 | GEO

A phenotypic screening platform for identifying chemical modulators of astrocyte reactivity

Project description:This SuperSeries is composed of the SubSeries listed below. Disease, injury, and aging induce pathological reactive astrocyte states that contribute to neurodegeneration. Modulating reactive astrocytes therefore represents an attractive therapeutic strategy. Here, we describe the development of an astrocyte phenotypic screening platform for identifying chemical modulators of astrocyte reactivity. Leveraging this platform for chemical screening, we identify HDAC3 inhibitors as effective suppressors of pathological astrocyte reactivity. We demonstrate that HDAC3 inhibition reduces molecular and functional characteristics of reactive astrocytes in vitro. Transcriptional and chromatin mapping studies show that HDAC3 inhibition disarms pathological astrocyte gene expression and function while promoting the expression of genes associated with beneficial astrocytes. Administration of RGFP966, a small molecule HDAC3 inhibitor, blocks reactive astrocyte formation and promotes neuroprotection in vivo in mice. Collectively, these results establish a platform for discovering modulators of reactive astrocyte states, inform the mechanisms that control astrocyte reactivity, and demonstrate the therapeutic benefits of modulating astrocyte reactivity for neurodegenerative diseases.

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A phenotypic screening platform for identifying chemical modulators of astrocyte reactivity [scRNAseq]

Project description:Disease, injury, and aging induce pathological reactive astrocyte states that contribute to neurodegeneration. Modulating reactive astrocytes therefore represents an attractive therapeutic strategy. Here, we describe the development of an astrocyte phenotypic screening platform for identifying chemical modulators of astrocyte reactivity. Leveraging this platform for chemical screening, we identify HDAC3 inhibitors as effective suppressors of pathological astrocyte reactivity. We demonstrate that HDAC3 inhibition reduces molecular and functional characteristics of reactive astrocytes in vitro. Transcriptional and chromatin mapping studies show that HDAC3 inhibition disarms pathological astrocyte gene expression and function while promoting the expression of genes associated with beneficial astrocytes. Administration of RGFP966, a small molecule HDAC3 inhibitor, blocks reactive astrocyte formation and promotes neuroprotection in vivo in mice. Collectively, these results establish a platform for discovering modulators of reactive astrocyte states, inform the mechanisms that control astrocyte reactivity, and demonstrate the therapeutic benefits of modulating astrocyte reactivity for neurodegenerative diseases.

2024-01-10 | GSE184437 | GEO

A phenotypic screening platform for identifying chemical modulators of astrocyte reactivity [BulkRNAseq.ONC]

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Divergent transcriptional regulation of astrocyte reactivity across disorders [TR_ATAC_SCI]

Project description:Single-nuclei Assay for Transposase-Accessible Chromatin with sequencing (snATACseq) was applied to examine chromatin landscape changes and transcriptional regulator (TR) DNA motif accessibility in reactive astrocytes following traumatic spinal cord injury (SCI). Astrocyte nuclei were isolated from the spinal cord of wild type mice and mice with astrocyte-specific conditional gene deletion (cKO) of test-case TRs, SMARCA4 (Smarca4-astro-cKO) or STAT3 knockout (Stat3-astro-cKO). Comparison of differential chromatin accessibility revealed substantial remodeling during astrocyte reactivity, with more chromatin opening than closing. Marked alterations in access to SCI reactivity-associated TR motifs were also detected.

2022-05-26 | GSE199481 | GEO

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